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Published on: April 10, 2018
Long non-coding RNA FENDRR inhibits NSCLC cell growth and aggressiveness by sponging miR-761
M-Y Zhang1, Z-L Zhang, H-X Cui
1Department of Thoracic Surgery, Affiliated Hospital of Weifang Medical University, Weifang, China. fulinfulinfl@163.com.
Objective:
The aim of this paper is to investigate the functions of long noncoding RNA (lncRNA) FOXF1 Adjacent Non-Coding Developmental Regulatory RNA (FENDRR) in the growth and aggressiveness of non-small cell lung cancer (NSCLC).
Patients And Methods:
The expression of FENDRR in NSCLC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and colony formation assays were conducted to explore the roles of FENDRR on the growth of NSCLC cell. The wound healing and transwell invasion assays were conducted to explore the impact of FENDRR on NSCLC cell migration and invasion. The apoptosis of NSCLC cell was detected using flow cytometer-based Annexin V/Propidium Iodide (PI) dual staining. The xenograft model was conducted to investigate the effect of FENDRR on the growth of NSCLC cell in vivo. The expression of Ki67 was measured by immunohistochemical (IHC) staining using Ki67 antibody. Bioinformatics analysis and Luciferase reporter assay were applied to identify that miR-761 was the target of FENDRR. Additional, colony formation and transwell experiments were utilized to confirm that FENDRR inhibited the growth and aggressiveness of NSCLC cell by regulating miR-761.
Results:
We found a marked down-regulation of FENDRR in NSCLC tissues compared to tumor-adjacent tissues. FENDRR down-expression was detected in four NSCLC cell lines (H1650, HCC827, H1975 and A549) compared to the human non-tumorigenic bronchial epithelial cell, BEAS-2B. Low expression of FENDRR was identified as a predictive factor for poor prognosis of patients with NSCLC. The over-regulation of FENDRR inhibited the proliferation, migration and invasion capacities of NSCLC cell and promoted the apoptosis of NSCLC cell in vitro whereas the down-regulation of FENDRR caused the opposite results. Moreover, the over-expression of FENDRR restrained the growth of NSCLC cell in vivo. We found that there were potential binding sites between FENDRR and miR-761 and the level of miR-761 was inversely associated with the expression of ENDRR in NSCLC tissues. Finally, the rescue experiments suggested that the anti-oncogenic role of FENDRR was at least partially mediated by miR-761 in NSCLC.
Conclusions:
We found that FENDRR was down-expressed in NSCLC and the over-expression of FENDRR inhibited the malignant phenotypes of NSCLC cell by binding to miR-761 competitively.
Insights
Long noncoding RNA (lncRNA) FENDRR is downregulated in non-small cell lung cancer (NSCLC). Its overexpression inhibits NSCLC growth and aggressiveness by competitively binding to miR-761, suggesting a tumor-suppressive role.
Area of Science:
- Molecular Biology
- Oncology
- RNA Biology
Background:
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality.
- Long noncoding RNAs (lncRNAs) play crucial roles in cancer development and progression.
- The specific role of FOXF1 Adjacent Non-Coding Developmental Regulatory RNA (FENDRR) in NSCLC remains largely unexplored.
Purpose of the Study:
- To investigate the expression and function of lncRNA FENDRR in non-small cell lung cancer (NSCLC).
- To elucidate the underlying molecular mechanisms by which FENDRR influences NSCLC growth, migration, invasion, and apoptosis.
- To identify potential therapeutic targets for NSCLC based on FENDRR's role.
Main Methods:
- Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) to assess FENDRR expression in NSCLC tissues and cell lines.
- In vitro assays including MTT, colony formation, wound healing, and transwell invasion to evaluate FENDRR's impact on NSCLC cell behavior.
- Flow cytometry for apoptosis analysis, xenograft models for in vivo tumor growth assessment, and immunohistochemistry for Ki67 expression.
- Bioinformatics analysis and luciferase reporter assays to identify and confirm miR-761 as a direct target of FENDRR.
Main Results:
- FENDRR was significantly downregulated in NSCLC tissues and cell lines compared to normal controls.
- Low FENDRR expression correlated with poor prognosis in NSCLC patients.
- Overexpression of FENDRR inhibited NSCLC cell proliferation, migration, and invasion while promoting apoptosis in vitro.
- FENDRR overexpression suppressed NSCLC tumor growth in vivo, evidenced by reduced Ki67 expression.
- FENDRR directly targets miR-761, and its tumor-suppressive effects are partially mediated through this interaction.
Conclusions:
- FENDRR acts as a tumor suppressor in NSCLC, exhibiting significantly lower expression in cancerous tissues.
- FENDRR overexpression inhibits NSCLC cell proliferation, migration, and invasion, and promotes apoptosis.
- The anti-oncogenic function of FENDRR in NSCLC is, at least partially, mediated by its competitive binding to miR-761.
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